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• W2015344530 abstract "Good et al present a fascinating case of a 38-year-old man with nephrotic-range proteinuria.1Good K.S. O’Brien K. Schulman G. Kerjaschki D. Fogo A.B. Unexplained nephrotic-range proteinuria in a 38-year-old man A case of “no change disease”.Am J Kidney Dis. 2004; 43: 933-938Abstract Full Text Full Text PDF PubMed Scopus (13) Google Scholar The biopsy findings were limited to largely intact foot processes with effacement noted in only 20% to 30% of the capillary loops.In the Discussion, they state that, “[i]n essentially all diseases with nephrotic-range proteinuria, there is damage to the visceral epithelial cells, effaced foot processes, and loss of slit diaphragms.”1Good K.S. O’Brien K. Schulman G. Kerjaschki D. Fogo A.B. Unexplained nephrotic-range proteinuria in a 38-year-old man A case of “no change disease”.Am J Kidney Dis. 2004; 43: 933-938Abstract Full Text Full Text PDF PubMed Scopus (13) Google Scholar Most proteinuric renal diseases such as diabetic nephropathy and focal segmental glomerulosclerosis have loss/effacement of podocyte foot processes. Furthermore, studies of congenital nephrotic syndromes caused by mutations of podocyte-specific proteins support the hypothesis that podocyte foot process effacement is the primary event that leads to proteinuria.2Mundel P. Shankland S.J. Podocyte biology and response to injury.J Am Soc Nephrol. 2002; 13: 3005-3015Crossref PubMed Scopus (573) Google Scholar, 3D’Amico G. Bazzi C. Pathophysiology of proteinuria.Kidney Int. 2003; 63: 809-825Crossref PubMed Scopus (358) Google Scholar However, as in this case report, there are both human and experimental models of nephrotic-range proteinuria in which podocyte foot process effacement is virtually absent. These include (1) glomerular endotheliosis, the characteristic lesion of human preeclampsia4Pirani C.L. Pollak V.E. Lannigan R. Folli G. The renal glomerular lesions of pre-eclampsia Electron microscopic studies.Am J Obstet Gynecol. 1963; 87: 1047-1070Abstract Full Text PDF PubMed Scopus (39) Google Scholar; (2) animal models of preeclampsia produced by sFlt-1 protein in rats5Maynard S.E. Min J.Y. Merchan J. et al.Excess placental soluble fms-like tyrosine kinase 1 (sFlt1) may contribute to endothelial dysfunction, hypertension, and proteinuria in preeclampsia.J Clin Invest. 2003; 111: 649-658Crossref PubMed Scopus (3093) Google Scholar; (3) “knock-out” mice in which glomerular vascular endothelial growth factor production has been reduced by 50%6Eremina V. Sood M. Haigh J. et al.Glomerular-specific alterations of VEGF-A expression lead to distinct congenital and acquired renal diseases.J Clin Invest. 2003; 111: 707-716Crossref PubMed Scopus (1065) Google Scholar; (4) rat model of proteinuria produced by injection of monoclonal antibody 5-1-67Orikasa M. Matsui K. Oite T. Shimizu F. Massive proteinuria induced in rats by a single intravenous injection of a monoclonal antibody.J Immunol. 1988; 141: 807-814PubMed Google Scholar; (5) Masugi nephritis model in rats8Kreisberg J.I. Wayne D.B. Karnovsky M.J. Rapid and focal loss of negative charge associated with mononuclear cell infiltration early in nephrotoxic serum nephritis.Kidney Int. 1979; 16: 290-300Crossref PubMed Scopus (58) Google Scholar; and (6) rare patients with familial nephrotic syndrome in whom podocytes are preserved.9Branten A.J. van den Born J. Jansen J.L. Assmann K.J. Wetzels J.F. Familial nephropathy differing from minimal change nephropathy and focal glomerulosclerosis.Kidney Int. 2001; 59: 693-701Crossref PubMed Scopus (35) Google Scholar A recent study of human biopsies with a variety of diseases showed no correlation between the degree of podocyte foot process effacement and proteinuria.10van den Berg J.G. van den Bergh Weerman M.A. Assmann K.J. Weening J.J. Florquin S. Podocyte foot process effacement is not correlated with the level of proteinuria in human glomerulopathies.Kidney Int. 2004; 66: 1901-1906Crossref PubMed Scopus (133) Google ScholarWe believe that effacement of foot processes occurs in many, but certainly not all, proteinuric diseases. Thus, the belief that the foot process and the slit diaphragm constitute the only barrier against proteinuria, and that their disruption is necessary for nephrotic-range proteinuria, is probably incorrect. ALL LETTERS TO THE EDITOR MUST BE SUBMITTED ONLINE VIA EDITORIAL MANAGER (http://ajkd.edmgr.com). Letters should be in response to an AJKD article, and that article should have appeared no more than 6 months previously. The title must be different from that of the original article. Letters must not exceed 250 words (excluding references, maximum number 10) and contain no more than 1 figure or table. Letters are subject to editing and abridgment without notice and there is no guarantee that your letter will be published. Submitting the letter constitutes your permission for its publication in any current or subsequent issue or edition of AJKD, in any form or media, now known or hereafter developed. Good et al present a fascinating case of a 38-year-old man with nephrotic-range proteinuria.1Good K.S. O’Brien K. Schulman G. Kerjaschki D. Fogo A.B. Unexplained nephrotic-range proteinuria in a 38-year-old man A case of “no change disease”.Am J Kidney Dis. 2004; 43: 933-938Abstract Full Text Full Text PDF PubMed Scopus (13) Google Scholar The biopsy findings were limited to largely intact foot processes with effacement noted in only 20% to 30% of the capillary loops. In the Discussion, they state that, “[i]n essentially all diseases with nephrotic-range proteinuria, there is damage to the visceral epithelial cells, effaced foot processes, and loss of slit diaphragms.”1Good K.S. O’Brien K. Schulman G. Kerjaschki D. Fogo A.B. Unexplained nephrotic-range proteinuria in a 38-year-old man A case of “no change disease”.Am J Kidney Dis. 2004; 43: 933-938Abstract Full Text Full Text PDF PubMed Scopus (13) Google Scholar Most proteinuric renal diseases such as diabetic nephropathy and focal segmental glomerulosclerosis have loss/effacement of podocyte foot processes. Furthermore, studies of congenital nephrotic syndromes caused by mutations of podocyte-specific proteins support the hypothesis that podocyte foot process effacement is the primary event that leads to proteinuria.2Mundel P. Shankland S.J. Podocyte biology and response to injury.J Am Soc Nephrol. 2002; 13: 3005-3015Crossref PubMed Scopus (573) Google Scholar, 3D’Amico G. Bazzi C. Pathophysiology of proteinuria.Kidney Int. 2003; 63: 809-825Crossref PubMed Scopus (358) Google Scholar However, as in this case report, there are both human and experimental models of nephrotic-range proteinuria in which podocyte foot process effacement is virtually absent. These include (1) glomerular endotheliosis, the characteristic lesion of human preeclampsia4Pirani C.L. Pollak V.E. Lannigan R. Folli G. The renal glomerular lesions of pre-eclampsia Electron microscopic studies.Am J Obstet Gynecol. 1963; 87: 1047-1070Abstract Full Text PDF PubMed Scopus (39) Google Scholar; (2) animal models of preeclampsia produced by sFlt-1 protein in rats5Maynard S.E. Min J.Y. Merchan J. et al.Excess placental soluble fms-like tyrosine kinase 1 (sFlt1) may contribute to endothelial dysfunction, hypertension, and proteinuria in preeclampsia.J Clin Invest. 2003; 111: 649-658Crossref PubMed Scopus (3093) Google Scholar; (3) “knock-out” mice in which glomerular vascular endothelial growth factor production has been reduced by 50%6Eremina V. Sood M. Haigh J. et al.Glomerular-specific alterations of VEGF-A expression lead to distinct congenital and acquired renal diseases.J Clin Invest. 2003; 111: 707-716Crossref PubMed Scopus (1065) Google Scholar; (4) rat model of proteinuria produced by injection of monoclonal antibody 5-1-67Orikasa M. Matsui K. Oite T. Shimizu F. Massive proteinuria induced in rats by a single intravenous injection of a monoclonal antibody.J Immunol. 1988; 141: 807-814PubMed Google Scholar; (5) Masugi nephritis model in rats8Kreisberg J.I. Wayne D.B. Karnovsky M.J. Rapid and focal loss of negative charge associated with mononuclear cell infiltration early in nephrotoxic serum nephritis.Kidney Int. 1979; 16: 290-300Crossref PubMed Scopus (58) Google Scholar; and (6) rare patients with familial nephrotic syndrome in whom podocytes are preserved.9Branten A.J. van den Born J. Jansen J.L. Assmann K.J. Wetzels J.F. Familial nephropathy differing from minimal change nephropathy and focal glomerulosclerosis.Kidney Int. 2001; 59: 693-701Crossref PubMed Scopus (35) Google Scholar A recent study of human biopsies with a variety of diseases showed no correlation between the degree of podocyte foot process effacement and proteinuria.10van den Berg J.G. van den Bergh Weerman M.A. Assmann K.J. Weening J.J. Florquin S. Podocyte foot process effacement is not correlated with the level of proteinuria in human glomerulopathies.Kidney Int. 2004; 66: 1901-1906Crossref PubMed Scopus (133) Google Scholar We believe that effacement of foot processes occurs in many, but certainly not all, proteinuric diseases. Thus, the belief that the foot process and the slit diaphragm constitute the only barrier against proteinuria, and that their disruption is necessary for nephrotic-range proteinuria, is probably incorrect. ALL LETTERS TO THE EDITOR MUST BE SUBMITTED ONLINE VIA EDITORIAL MANAGER (http://ajkd.edmgr.com). Letters should be in response to an AJKD article, and that article should have appeared no more than 6 months previously. The title must be different from that of the original article. Letters must not exceed 250 words (excluding references, maximum number 10) and contain no more than 1 figure or table. Letters are subject to editing and abridgment without notice and there is no guarantee that your letter will be published. Submitting the letter constitutes your permission for its publication in any current or subsequent issue or edition of AJKD, in any form or media, now known or hereafter developed. ALL LETTERS TO THE EDITOR MUST BE SUBMITTED ONLINE VIA EDITORIAL MANAGER (http://ajkd.edmgr.com). Letters should be in response to an AJKD article, and that article should have appeared no more than 6 months previously. The title must be different from that of the original article. Letters must not exceed 250 words (excluding references, maximum number 10) and contain no more than 1 figure or table. Letters are subject to editing and abridgment without notice and there is no guarantee that your letter will be published. Submitting the letter constitutes your permission for its publication in any current or subsequent issue or edition of AJKD, in any form or media, now known or hereafter developed. ALL LETTERS TO THE EDITOR MUST BE SUBMITTED ONLINE VIA EDITORIAL MANAGER (http://ajkd.edmgr.com). Letters should be in response to an AJKD article, and that article should have appeared no more than 6 months previously. The title must be different from that of the original article. Letters must not exceed 250 words (excluding references, maximum number 10) and contain no more than 1 figure or table. Letters are subject to editing and abridgment without notice and there is no guarantee that your letter will be published. Submitting the letter constitutes your permission for its publication in any current or subsequent issue or edition of AJKD, in any form or media, now known or hereafter developed." @default.
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